Telomeres shorten each time a cell divides to make a new cell, until they become inactive.

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QIMR researchers have helped find new evidence that links faster ‘biological’ ageing to the risk of developing several age-related diseases―including heart disease, multiple sclerosis and various cancers.

Dr Dale Nyholt, from QIMR’s Neurogenetics laboratory, said the international study of more than 48,000 people studied a feature of our chromosomes called telomeres, which wear down at varying speeds.

“These are really exciting findings, which open the possibility that manipulating telomere length could have health benefits,” Dr Nyholt said.

Telomeres sit on the end of our chromosomes―the strands of DNA stored in the nucleus of cells. Telomeres shorten each time a cell divides to make new cells, until they reach a critical short length and the cells enter an inactive state and die. So telomeres shorten as an individual gets older. But individuals are born with different telomere lengths and the rate at which they subsequently shorten can also vary. The speed with which telomeres wear down is a measure of ‘biological ageing’.

“Although heart disease and cancers are more common as one gets older, not everyone gets them, and some people get them at an earlier age. We suspected that these diseases may in part be related to some people “biologically” ageing more quickly than others,” Dr Nyholt said.

The research team measured people’s telomere lengths, looked at their DNA and identified seven genetic variants that were associated with telomere length. They then determined that those variants were also linked to several types of cancers, including colorectal cancer, as well as diseases like multiple sclerosis and coeliac disease.

The team also found that the seven variants were associated with risk of coronary artery disease which can lead to heart attacks.

“This research strongly suggests that biological ageing plays an important role in causing coronary artery disease, the most common cause of death in the world. This provides a new way of looking at the disease and at least partly explains why some patients develop it early and others don’t develop it at all even if they carry other risk factors.”

The study, led by the University of Leicester, UK, involved scientists from 14 organisations across eight countries, working as part of the European ENGAGE Consortium. It is published in Nature Genetics and available here.